Latest Research – Fortinberry Murrayhttp://fortinberrymurray.com
Bringing your best future forwardTue, 13 Mar 2018 22:55:42 +0000en-UShourly1Watching others makes people overconfident in their own abilities.http://fortinberrymurray.com/todays-research/watching-others-makes-people-overconfident-in-their-own-abilities/
Tue, 13 Mar 2018 22:55:42 +0000http://fortinberrymurray.com/?p=4115Watching YouTube videos, Instagram demos, and Facebook tutorials may make us feel as though we’re acquiring all sorts of new skills but it probably won’t make us experts, according to research published in Psychological Science.

“The more that people watched others, the more they felt they could perform the same skill, too—even when their abilities hadn’t actually changed for the better,” says the study lead author.… [read more]

]]>Watching YouTube videos, Instagram demos, and Facebook tutorials may make us feel as though we’re acquiring all sorts of new skills but it probably won’t make us experts, according to research published in Psychological Science.

“The more that people watched others, the more they felt they could perform the same skill, too—even when their abilities hadn’t actually changed for the better,” says the study lead author. “Our findings suggest that merely watching others could cause people to attempt skills that they might not be ready or able to perform themselves.”

Social media platforms have made it easy to record, share, and access instructional videos. But does watching videos without practicing the demonstrated skills actually improve our ability to perform them?

In one online experiment, the researchers assigned 1,003 participants to watch a video, read step-by-step instructions, or merely think about performing the “tablecloth trick,” which involves pulling a tablecloth off a table without disturbing the place settings on top. People who watched the 5-second video 20 times were much more confident in their ability to pull off the trick than were those who watched the video once. However, people who simply read or thought about the trick for an extended period of time did not show this confidence boost. These results provided initial evidence that repeated viewing may lead people to an inflated sense of competence.

To find out whether this perception is borne out by actual performance, the researchers tested a group of 193 participants on their dart-throwing abilities. Those who watched a demo video 20 times estimated that they would score more points than those who saw the video only once—this high-exposure group also predicted that they would be more likely to hit the bull’s-eye and reported that they had learned more technique and improved more after watching the video.

But these perceptions did not line up with reality: People who watched the video many times scored no better than those who saw it once.

The researchers found evidence for this phenomenon in other domains, including doing the moonwalk, playing a digital computer game, and juggling. The more that participants watched others perform these skills, the more they overestimated their own abilities.

Why does repeatedly watching a video breed such overconfidence? Participants who watched a variation of the tablecloth trick video that did not show the performer’s hands evidenced no exposure-related overconfidence, suggesting that people may feel confident only when they can track the specific steps and actions in performing a skill.

Thinking about detailed steps or learning technical information about the objects involved did not lead participants to form more accurate perceptions. In an experiment focused on juggling, only participants who were able to hold the pins after watching a juggling video revised their estimates, reporting that they had learned less and were less capable than they originally thought after watching.

“We see this as a potentially widespread phenomenon given that people have daily access to outlets for watching others perform,” said the team. “Anyone who goes online to look up tips before attempting a skill – from cooking techniques to DIY home repairs to X Games tricks – would benefit from knowing that they might be overconfident in their own abilities after watching and should exercise caution before attempting similar skills themselves.”

So, what? The lesson here is that watching the videos only increases the natural human trait to overestimate one’s own abilities. A lot of teaching methods—in industry and elsewhere—are going to have to be revised.

]]>Frequent ‘I-Talk’ may signal proneness to emotional distresshttp://fortinberrymurray.com/todays-research/frequent-i-talk-may-signal-proneness-to-emotional-distress/
Tue, 13 Mar 2018 22:52:42 +0000http://fortinberrymurray.com/?p=4113I met with a potential coaching client the other day. He was a member of the C-suite of a large listed company. He couldn’t stop talking about himself. Everything in his life revolved around him and he seemed incapable of seeing anything from anyone else’s perspective.… [read more]

]]>I met with a potential coaching client the other day. He was a member of the C-suite of a large listed company. He couldn’t stop talking about himself. Everything in his life revolved around him and he seemed incapable of seeing anything from anyone else’s perspective. He is by no means unusual. The conversation with this man kept swirling around my head as I read this very interesting study.

What the researchers say: We all know someone who seems to really enjoy talking about him—or herself. Yet while the chorus of “I, I, I” and “me, me, me” might convince us we are conversing with a classic narcissist, the researchers suggest we shouldn’t be so quick to judge.

They found in an earlier study that frequent use of first-person singular pronouns – I me and my – is not, in fact, necessarily an indicator of narcissism.

Instead, this so-called “I-talk” may signal that someone is prone to emotional distress, according to a new, follow-up study in the Journal of Personality and Social Psychology.

Previous studies have suggested that I-talk, though not an indicator of narcissism, may be a marker for depression. While the new study confirms that link, the researchers found an even greater connection between high levels of I-talk and a link to negative emotionality in general.

Negative emotionality refers to a tendency to easily become upset or emotionally distressed, whether that means experiencing depression, anxiety, worry, tension, anger or other negative emotions.

The researchers found that when people talk a lot about themselves, it could point to depression, but it could just as easily indicate that they are prone to anxiety or any number of other negative emotions. Therefore, I-talk shouldn’t be considered a marker for depression alone.

“The question of whether I-talk reflects depression more specifically, or negative affect more broadly, was a really important question because if you’re thinking of using I-talk as a screening tool, you want to know if it screens specifically for a risk for depression or if it screens more broadly for a tendency to experience negative affect, which is a broader risk factor for a suite of mental health concerns,” the lead author said.

The researchers’ findings are based on a large dataset of more than 4,700 individuals from six labs in two countries – the U.S. and Germany. The data included measures of individuals’ use of I-talk – either in written or spoken tasks – as well as measures of depression and negative emotionality.

“Previous research had found the one link – between I-talk and depression – but it hadn’t examined moderators in great detail in a large sample. That was the next step,” he said. “Our results suggest that I-talk may not be very good at assessing depression in particular. It may be better at assessing a proneness not just to depression but to negative emotionality more broadly.”

So how much I-talk is considered a lot? The average person speaks about 16,000 words a day, about 1,400 of which are, on average, first-person singular pronouns, the researchers noted. Those prone to distress may say “I, me and my” up to 2,000 times a day.

Researchers also looked at whether gender and communication context affected the relationship between I-talk and negative emotionality. They found that gender does not play an important role but communication context does.

“If you are speaking in a personal context – so you’re speaking about something that’s of relevance to you, like a recent breakup – then we see the relationship between I-talk and negative emotionality emerge,” they said. “But if you’re communicating in a context that’s more impersonal, such as describing a picture, we did not see the relationship emerge.”

In addition, the researchers found that the specific type of first-person singular pronoun made a difference. Frequent use of the subjective first-person pronoun “I” and the objective first-person pronoun “me” was linked to negative emotionality, but frequent use of the first-person possessive pronoun “my” was not. That may be because “my” connects a person to another individual or object on the “outside,” effectively taking the “psychological spotlight” off the self they said.

“We’ve all gone through negative life events when we’re feeling down or we’re feeling anxious, and when you think back to being in those places, when you’re just so focused on yourself, you may say things like ‘Why can’t I get better?’” the lead author said. “You’re so focused on yourself that not only in your head are you using these first-person singular pronouns but when you’re talking to other people or writing, it spills into your language – the self-focus that negative affectivity brings about.”

As the lead researcher says, regarding the research: “Stress can make you be caught in the metaphorical ‘I’ of the storm.”

So, what? We’re often too quick to make judgements about people and to label them as being this or that. People who seem fixated on themselves we often tend to class as narcissists whereas they may just be overstressed or depressed or anxious. Often this misdiagnosis can lead to someone not being offered a job, or not hired in the first place.

This study is a good corrective and should be remembered before we rush to judgement.

]]>In a remarkable study researchers have discovered that stress isn’t just contagious; it alters the brain on a cellular level.

In the study, published in Nature Neuroscience, researchers have discovered that stress transmitted from others can change the brain in the same way as a real stress does. The study, in mice, also shows that the effects of stress on the brain are reversed in female mice following a social interaction. This was not true for male mice.

What the researchers say: “Brain changes associated with stress underpin many mental illnesses including PTSD, anxiety disorders and depression,” says the lead author. “Recent studies indicate that stress and emotions can be ‘contagious’. Whether this has lasting consequences for the brain is not known.”

The team studied the effects of stress in pairs of male or female mice. They removed one mouse from each pair and exposed it to a mild stress before returning it to its partner. They then examined the responses of a specific population of cells, specifically CRH neurons which control the brain’s response to stress, in each mouse, which revealed that networks in the brains of both the stressed mouse and naïve partner were altered in the same way.

What was remarkable was that CRH neurons from the partners, who were not themselves exposed to an actual stress, showed changes that were identical to those they measured in the stressed mice.

Next, the team used optogenetic (optogenetics is a biological technique which involves the use of light to control cells in living tissue) approaches to engineer these neurons so that they could either turn them on or off with light. When the team silenced these neurons during stress, they prevented changes in the brain that would normally take place after stress. When they silenced the neurons in the partner during its interaction with a stressed individual, the stress did not transfer to the partner. Remarkably, when they activated these neurons using light in one mouse, even in the absence of stress, the brain of the mouse receiving light and that of the partner were changed just as they would be after a real stress.

The team discovered that the activation of these CRH neurons causes the release of a chemical signal, an ‘alarm pheromone,’ from the mouse that alerts the partner. The partner who detects the signal can in turn alert additional members of the group. This propagation of stress signals reveals a key mechanism for transmission of information that may be critical in the formation of social networks in various species (including humans).

Another advantage of social networks is their ability to buffer the effects of adverse events. The team also found evidence for buffering of stress, but this was selective. They noticed that in females the residual effects of stress on CRH neurons were cut almost in half following time with unstressed partners. The same was not true for males.

The researchers suggest that these findings also apply to humans. “We readily communicate our stress to others, sometimes without even knowing it. There is even evidence that some symptoms of stress can persist in colleagues, family and loved ones of individuals who suffer from anxiety. On the flip side, the ability to sense another’s emotional state is a key part of creating and building social bonds.”

This research indicates that stress and social interactions are intricately linked. The consequences of these interactions can be long-lasting and may influence behaviors even decades later.

So, what? That females and males differ in their reactions to stress has been known for a long time (see previous TRs), as is the fact that stress is contagious (again see previous TRs). But that experiencing stress—even mild stress—can change the brain of a colleague or partner on the cellular level is quite bind-blowing. It explains the neural mechanism of things which I have observed and written about such as depression clusters in organizations, and even stressed or depressed companies, firms, or even societies.

The importance of this can’t be overemphasized. As the rate of workplace stress increases—as it is predicted to do—then the problem of contagious stress will also increase. In men this will lead to increased bullying and anger, and in both sexes to increased fear and loathing of anyone perceived as “different”(as is reported in another study this week).

What now? No amount of training and persuasion will help reverse the present trend towards increased mental ill-health and behavioral problems in workplaces. The only thing that will help is for companies and other organizations—and societies—to work together to lessen the fear and stress load on human beings

]]>Does ketamine really work as an antidepressant?http://fortinberrymurray.com/todays-research/does-ketamine-really-work-as-an-antidepressant/
Tue, 06 Mar 2018 22:29:44 +0000http://fortinberrymurray.com/?p=4100Antidepressant response within hours, or a blind alley? Experts weigh evidence on ketamine as a fast-acting treatment for depression in Harvard Review of Psychiatry.

Recent studies suggest that ketamine, a widely used anesthetic agent, could offer a wholly new approach to treating severe depression—producing an antidepressant response in hours rather than weeks.… [read more]

]]>Antidepressant response within hours, or a blind alley? Experts weigh evidence on ketamine as a fast-acting treatment for depression in Harvard Review of Psychiatry.

Recent studies suggest that ketamine, a widely used anesthetic agent, could offer a wholly new approach to treating severe depression—producing an antidepressant response in hours rather than weeks. Two reviews of recent evidence on ketamine and related drugs for treating depression appear in the journal.

In one paper the researchers at the National Institute of Mental Health claim that ketamine and related drugs may represent a “paradigm shift” in the treatment of major depressive disorder (MDD) and bipolar depression—especially in patients who do not respond to other treatments.

A second article explores the evidence on the mechanisms behind ketamine’s rapid antidepressant effects.

Current treatments for MDD and bipolar depression have major limitations. Most patients with severe depressive symptoms don’t respond to available antidepressant drugs. Even for those who do respond, it may take several weeks before symptoms improve.

Ketamine is one of several glutamatergic drugs (i.e. those that target the glutamate system) affecting neurotransmitters in the central nervous system. Over the past decade, several studies have reported “rapid, robust, and relatively sustained antidepressant response” to ketamine, injected intravenously at low, subanesthetic doses.

Ketamine may also rapidly reduce suicidal thoughts and has become a first-line treatment for suicidality in many countries. Combined with other medications, ketamine has also produced rapid antidepressant effects in patients with treatment-resistant bipolar depression.

Prompted by these studies, some doctors are already using ketamine in patients with severe or treatment-resistant depression. However, since it is FDA-approved only as an anesthetic, use of ketamine in depressive disorders is “off-label,” unregulated, and not standardized. Many questions remain about its short- and long-term side effects and potential for abuse (in a refined form it is a street drug called “special K”).

“Efforts are underway to bring ketamine to market, standardize its use, and determine its real-world effectiveness,” the NIH coauthors write. They also present evidence on several other glutamatergic drugs. One drug, esketamine, has been given “breakthrough therapy” status by the FDA for patients at imminent risk of suicide.

Researchers from the Massachusetts General Hospital reviewed neuroimaging studies evaluating ketamine’s effects in the brain. The studies show ketamine-induced changes in several brain areas involved in the development of depression. Ketamine may exert its antidepressant effects by “acutely disabling the emotional resources required to perpetuate the symptoms of depression,” as well as by increasing emotional blunting and increasing activity in reward processing.

Independent of how ketamine works or its ultimate role in clinical treatment, antidepressant response to glutamatergic drugs points to an exciting conclusion: “that rapid antidepressant effects are indeed achievable in humans,” they write. “This paradigm shift lends additional urgency to the development of novel treatments for MDD and bipolar depression, particularly for patient subgroups that do not respond to currently available therapies.”

So what? At the present time we know that ketamine and similar drugs are an excellent immediate therapy for suicidal patients or those whose MDD is too severe fort them to operate in the world. We know nothing of its medium-to-long term effects but it is an exciting area for further study. What we do know is that, at least in the very short term, it works for everyone with severe depression. That’s the very good news.

]]>New method helps identify causal mechanisms in depression.http://fortinberrymurray.com/todays-research/new-method-helps-identify-causal-mechanisms-in-depression/
Tue, 06 Mar 2018 22:16:33 +0000http://fortinberrymurray.com/?p=4097A new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging looks at the driving influence of brain regions in depression.What the researchers say: The researchers note that people with major depressive disorder have alterations in the activity and connectivity of brain systems underlying reward and memory.… [read more]

]]>A new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging looks at the driving influence of brain regions in depression.What the researchers say: The researchers note that people with major depressive disorder have alterations in the activity and connectivity of brain systems underlying reward and memory. The findings provide clues as to which regions of the brain could be at the root of depressive symptoms, such as reduced happiness and pleasure.

The research uses a new approach to measure the influence of one brain region on another, referred to as effective connectivity, in depression. The approach goes beyond the limitations of previous brain imaging studies, which show if—but not how—activity of different brain regions is related. “The new method allows the effect of one brain region on another to be measured in depression, in order to discover more about which brain systems make causal contributions to depression,” said the lead researcher.

“This represents an exciting new methodological advance in the development of diagnostic biomarkers and the identification of critical brain circuitry for targeted interventions for major depression,” he added.

The team compared 336 people with major depressive disorder to 350 healthy controls. Brain regions involved in reward and subjective pleasure received less drive (or reduced effective connectivity) in depressed patients, which may contribute to the decreased feeling of happiness in depression.

In addition, brain regions involved in punishment and responses when a reward is not received had decreased effective connectivity and increased activity, providing evidence for the source of sadness that occurs in the disorder.

Memory-related areas of the brain had increased activity and connectivity in people with depression, which the authors suggest may be related to heightened memory processing, possibly of unpleasant memories, in depression.

“These findings are part of a concerted approach to better understand the brain mechanisms related to depression, and thereby to lead to new ways of understanding and treating depression,” said the researchers.

So what? This study, together with the first one reported here, show that there is an increasing interest in the connectivity of the brain in the development of depression—or at least some depression since there are potentially many, many, forms of the disease. Certainly the idea of looking at the connectivity that underlies the experience—or lack of experience—of pleasure or the inability to remember pleasurable things or experiences is novel. If depression really is a collection of diverse symptoms with a zillion possible origins then it makes perfect sense to target the symptomology since the underlying cause—biological or experiential—may be impossible to identify or treat in any individual.

]]>A pathway to a better way to treat depression?http://fortinberrymurray.com/todays-research/a-pathway-to-a-better-way-to-treat-depression/
Tue, 06 Mar 2018 22:12:47 +0000http://fortinberrymurray.com/?p=4095About 30-40% of depression is genetic in origin. A really interesting study just published outlines a new and rather dramatic look at this aspect of depression. Essentially it indicates that all current treatments are looking at the wrong areas of the brain and therefore that is the reason all existing treatments fail so many sufferers.… [read more]

]]>About 30-40% of depression is genetic in origin. A really interesting study just published outlines a new and rather dramatic look at this aspect of depression. Essentially it indicates that all current treatments are looking at the wrong areas of the brain and therefore that is the reason all existing treatments fail so many sufferers.

What the researchers say: The new research shows that individuals with high levels of a little-studied neural receptor called GPR158 may be more susceptible to depression following chronic stress.

“The next step in this process is to come up with a drug that can target this receptor,” said the lead researcher. His team zeroed in on GPR158 as a player in depression after discovering that the protein linked it its specialized receptors, and thus to the gene, is elevated in people with major depressive disorder. To better understand GPR158’s role, the scientists studied male and female mice with and without GPR158 receptors.

Behavioral tests revealed that both male and female mice with active GPR158 receptors show signs of depression following chronic stress. On the flip side, suppression of GPR158 protects mice from developing depressive-like behaviors and make them resilient to stress.

Next, the researchers examined why GPR158 has these effects on depression. The team demonstrated that GPR158 affects key signaling pathways involved in mood regulation in the prefrontal cortex (the thinking and reasoning part of the brain), though the researchers emphasized that the exact mechanisms remain to be established.

The lead author explains that GPR158 is a so-called “orphan receptor” (which gets its name because its binding partner/partners are unknown) with a poorly understood biology and mechanism of action. GPR158 appears to work downstream from other important brain systems, such as the GABA system (GABA is the most prevalent neurochemical in the brain), a major player in the brain’s inhibitory control and adrenergic system involved in our reaction to stress.

“This is really new biology and we still need to learn a lot,” say the researchers.

The study also offers a potential clue to why some people are more susceptible to mental illness. Because mice without GPR158 don’t alter their behavior after chronic stress, the researchers concluded these mice were naturally more resilient against depression. Their genetics, or more precisely their gene expression, offer a layer of protection.

The researchers say this finding matches what doctors have noticed in people who have experienced chronic stress. “There’s always a small population that is resilient—they don’t show the depressive phenotype.”

As the search goes on for additional targets for depression, scientists are increasingly using new tools in genome analysis to identify orphan receptors like GPR158. “Those are the untapped biology of our genomes, with significant potential for development of innovative therapeutics,” the team says.

So what? It’s well possible—indeed almost certain—that there are many genetic pathways to depressive illness. The genes that control the neurochemicals dopamine, oxytocin, serotonin and glutamate are all suspects which are “helping the (depression) police with their enquiries.”GPR158 is another. All of these genes are affected by stress and it could be that GPR158 in some way amplifies the effects of stressful events.

The other really fascinating point of this study is that it shows that resilience is largely inherited—an argument that I have been making in academic and business circles for over two decades.

]]>Depression changes the brain over time.http://fortinberrymurray.com/todays-research/depression-changes-the-brain-over-time/
Tue, 06 Mar 2018 22:05:23 +0000http://fortinberrymurray.com/?p=4093Over years, depression quite literally changes the brain, new research shows. Importantly the researchers found that persistent depression may need a different therapeutic approach from all those that have been tried so far. They findings also raised the question: Is clinical depression always the same illness, or does it change over time?… [read more]

]]>Over years, depression quite literally changes the brain, new research shows. Importantly the researchers found that persistent depression may need a different therapeutic approach from all those that have been tried so far. They findings also raised the question: Is clinical depression always the same illness, or does it change over time?

What the researchers say: New brain imaging research shows that the brain alters after years of persistent depression, suggesting the need to change how we think about depression as it progresses.

The research shows that people with longer periods of untreated depression, lasting more than a decade, had significantly more brain inflammation compared to those who had less than 10 years of untreated depression. In an earlier study the team discovered the first definitive evidence of inflammation in the brain in clinical depression.

This study provides the first biological evidence for large brain changes in long-lasting depression, suggesting that it is a different stage of illness that needs different therapeutics—the same perspective taken for early and later stages of Alzheimer’s disease, the lead author says.

“Greater inflammation in the brain is a common response with degenerative brain diseases as they progress, such as with Alzheimer’s disease and Parkinson´s disease,” he says. While depression is not considered a degenerative brain disease, the change in inflammation shows that, for those in whom depression persists, it may be progressive and not a static condition.

Yet currently regardless of how long a person has been ill, major depressive disorder is mainly treated with the same approach. Some people may have a couple of episodes of depression over a few years. Others may have persistent episodes over a decade with worsening symptoms, including increasing difficulty going to work or carrying out routine activities.

Treatment options for this later stage of illness, such as medications targeting inflammation, are being investigated (see recent TRs). This includes re-purposing current medications designed for inflammation in other illnesses to be used in major depressive disorder.

In the study, brain inflammation was measured using a type of brain imaging called positron emission tomography (PET). The brain’s immune cells, known as microglia, are involved in the brain’s normal inflammatory response to trauma or injury, but too much inflammation is associated with degenerative illnesses as well as depression.

The study involved 25 people with more than 10 years of depression, 25 with less than 10 years of illness, and 30 people with no depression as a comparison group. Inflammation levels were about 30 per cent higher in different brain regions among those with long-lasting untreated depression, compared to those with shorter periods of untreated depression. The group with long-term depression also had higher inflammation levels than those with no depression.

The researchers also note that in treatment studies, patients with serious, longstanding depression tend to be excluded, so there is a lack of evidence of how to treat this stage of illness, which needs to be addressed.

So what? Treating depression with anti-inflammatory drugs is not a new idea. Nor is the idea that depression can increase in severity with age. What is new in this study is the idea that the two are linked and that depression becomes something very different involving changes in the way the brain functions over time. This will hopefully lead to the discovery of new and better treatments for people with long-standing depression—which is actually most depression sufferers of major depressive disorder over the age of 40.

]]>Stress, depression and memory decline.http://fortinberrymurray.com/todays-research/stress-depression-and-memory-decline/
Tue, 06 Mar 2018 22:04:29 +0000http://fortinberrymurray.com/?p=4091Undoubtedly the most important study on depression for a very long time was published this week. For the first time the causal link was established between stress—in our time this is mainly work stress—and depression.

]]>Undoubtedly the most important study on depression for a very long time was published this week. For the first time the causal link was established between stress—in our time this is mainly work stress—and depression.

Depression is associated with impaired recollection. People who are depressed have poor memory for positive events, and enhanced memory for negative events, but the relevant neural mechanisms are poorly understood. This is the focus of this new study in the journal Trends in Neurosciences.

What the researchers found. Stress is a common trigger of nearly all initial depressive episodes, and chronic (ongoing) stress can prevent new cells being formed in the hippocampus—the brain’s memory center—to replace those that have died off. This stress can also, they found, inhibit mesolimbic dopamine neurons (thus prevent sufferers from feeling pleasure), and sensitize the amygdala’s response to negative information. The amygdala is the main fear center of the brain and this sensitization tends to make people feel anxious and fearful and more likely to look for what’s wrong rather than what’s right.

So what? As our society becomes increasingly stressful the rate of depression increases. Some recent studies have shown that up to 30% of employees suffer from episodes of major depression. That is up from about 8% or so fifteen years ago. The stress produced by the way we are forced to work—including open plan offices and the like, the fear of job loss, the isolation of working from home, over work, being “on” via smartphone 24/7—is a major stressor. We are simply not designed to cope with it. Now we know for sure that this is, quite literally, killing us through the stress/depression nexus (often disguised as psychosomatic illness or very real heart disease).

]]>Self-compassion may protect people from the harmful effects of perfectionismhttp://fortinberrymurray.com/todays-research/self-compassion-may-protect-people-harmful-effects-perfectionism/
Sun, 25 Feb 2018 22:55:00 +0000http://fortinberrymurray.com/?p=4077I have a love of perfectionism—in its place. My partner Alicia is a great writer because she is a perfectionist. One of her articles will be written, rewritten and then completely rewritten again. In other areas of activity perfectionism is better left to machines.… [read more]

]]>I have a love of perfectionism—in its place. My partner Alicia is a great writer because she is a perfectionist. One of her articles will be written, rewritten and then completely rewritten again. In other areas of activity perfectionism is better left to machines.

We know from a great deal of previous research that perfectionism is closely linked to depression. This is the reason that lawyers, who tend to be perfectionistic, are also one of the most depressed groups of professionals.

What the researchers say: Relating to oneself in a healthy way can help weaken the association between perfectionism and depression, according to a study published in the journal PLOS ONE.

Perfectionistic people often push themselves harder than others to succeed but can also fall into the trap of being self-critical and overly concerned about making mistakes. When the perfectionist fails, they often experience depression and burnout. In this study the researchers considered whether self-compassion, a kind way of relating to oneself, might help temper the link between perfectionist tendencies and depression.

The researchers administered anonymous questionnaires to assess perfectionism, depression, and self-compassion across 541 adolescents and 515 adults. Their analyses of these self-assessments revealed than self-compassion may help uncouple perfectionism and depression.

The replication of this finding in two groups of differently-aged people suggests that self-compassion may help moderate the link between perfectionism and depression across the lifespan. The authors suggest that self-compassion interventions could be a useful way to undermine the effects of perfectionism, but future experimental or intervention research is needed to fully assess this possibility.

“Self-compassion, the practice of self-kindness, consistently reduces the strength of the relationship between maladaptive perfectionism and depression for both adolescents and adults,” says the lead author.

So what? I am sure they’re right, however I think the issue of the link between perfectionism and depression is a lot more complex than presented. For a start there is a great deal of genetic predisposition in perfectionism—as there is with OCD (obsessive compulsive disorder) with which it shares some symptomology.

Then again self-compassion—as a lot of previous research has shown—is perhaps a fiction. We get a sense of self-worth largely from the outside (the rest is genetic). From people showing that they value us, that they appreciate us and that they support us.

The other problem is that perfectionism can be a product of this externally-induced self-compassion. For example, if as a child a person had been praised for getting things right and punished for being wrong that person will get their sense of self-worth—and thus self-compassion—from that praise and will be afraid of being wrong or “imperfect.” They will love themselves for being right and show no self-compassion if they’re wrong.

]]>Pro-diversity policies make companies more innovative and profitable.http://fortinberrymurray.com/todays-research/pro-diversity-policies-make-companies-innovative-profitable/
Sun, 25 Feb 2018 22:51:15 +0000http://fortinberrymurray.com/?p=4075Sometimes research studies come along and fulfil a very useful role—proving the obvious. This is one of them, so it is to be greatly welcomed.

What the researchers say: While some may see corporate diversity initiatives as nothing more than glitzy marketing campaigns, the latest research shows that companies that hire a more diverse set of employees are rewarded with a richer pipeline of innovative products and a stronger financial position.… [read more]

]]>Sometimes research studies come along and fulfil a very useful role—proving the obvious. This is one of them, so it is to be greatly welcomed.

What the researchers say: While some may see corporate diversity initiatives as nothing more than glitzy marketing campaigns, the latest research shows that companies that hire a more diverse set of employees are rewarded with a richer pipeline of innovative products and a stronger financial position.

A variety of businesses large and small have launched initiatives to attract a more diverse and inclusive workforce. But no one has measured how diverse business practices impact a company’s bottom line. In this paper published in the journal Financial Management the researchers attempt to measure diversity’s impact on Corporate America.

The study showed that companies that promote a diverse workforce and a culture of inclusion, specifically attracting and retaining minorities, women, the disabled and LGBTQ employees, were more efficient in generating new products and patents. They found that diverse hiring practices increase the pool from which a firm can recruit talented and creative employees. The wider the range of views and backgrounds, experiences and expertise the company attracted, they concluded, the more innovative the company was to solve problems. A diverse, inclusive culture attracts and retains talent and boosts employee morale, the research found.

The team scoured and analyzed data on publicly traded U.S. firms, looking at new product introductions, patents and other company milestones. They showed that pro-diversity policies enhance future firm value by spurring innovation.

“Top corporate leaders, academics and policy makers have long been wondering about the real economic benefits of corporate diversity policies,” said the lead researcher. “Many didn’t see how hiring a more diverse workforce positively affected shareholder value. Now we have strong evidence that creating a more diverse workplace today results in more innovative outcomes for companies tomorrow.”

Her findings also showed that companies with pro-diversity policies weathered the 2008 economic downturn far better than those without them.

So what? This is an important paper because it shows that companies need to concentrate on hiring not just more of one set of “minorities” but rather people from a broad range of backgrounds and experiences.

Too many businesses have been fixated just on hiring more women. But women from the same socio-economic and ethnic background as the men will solve nothing as far as innovation is concerned (though increasing the number of women at senior levels is good in itself—if only because they make better leaders).

What now? Businesses should look at their hiring practices and ask themselves: are we getting the broadest range of viewpoints, experiences and talent that we possibly can?

Oh, and by the way, as the latest research on biased AI has shown—junk the multiple data-based machine hiring and use what humans have that machines never will have, an almost infallible gut judgement.